Evidence map›Paper›PMID 36300321›Full record

ArticleJournal of Korean Neurosurgical Society2023

Nicotinamide Mononucleotide Adenylyl Transferase 2 Inhibition Aggravates Neurological Damage after Traumatic Brain Injury in a Rat Model.

Xiaoyu Gu, Haibo Ni, XuGang Kan, Chen Chen, Zhiping Zhou, Zheng Ding, Di Li, Bofei Liu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of Korean Neurosurgical Society, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 56% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Xiaoyu GuDepartment of Intensive Care Unit, The Affiliated Zhangjiagang Hospital of Soochow University, Suzhou, China.
Haibo NiDepartment of Neurosurgery, The Affiliated Zhangjiagang Hospital of Soochow University, Suzhou, China.
XuGang KanDepartment of Neurobiology, The Affiliated Xuzhou Medical University, XuZhou, China.
Chen ChenDepartment of Intensive Care Unit, The Affiliated Zhangjiagang Hospital of Soochow University, Suzhou, China.
Zhiping ZhouDepartment of Orthopedics, The Affiliated Zhangjiagang Hospital of Soochow University, Suzhou, China.
Zheng DingDepartment of Intensive Care Unit, The Affiliated Zhangjiagang Hospital of Soochow University, Suzhou, China.
Di LiDepartment of Intensive Care Unit, The Affiliated Zhangjiagang Hospital of Soochow University, Suzhou, China.
Bofei LiuDepartment of Intensive Care Unit, The Affiliated Zhangjiagang Hospital of Soochow University, Suzhou, China.
Soochow University · CNXuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveNicotinamide mononucleotide adenylyl transferase 2 (NMNAT2) is a crucial factor for the survival of neuron. The role of NMNAT2 in damage following traumatic brain injury (TBI) remains unknown. This study was designed to investigate the role of NMNAT2 in TBI-induced neuronal degeneration and neurological deficits in rats.

methodsThe TBI model was established in Sprague-Dawley rats by a weight-dropping method. Real-time polymerase chain reaction, western blot, immunofluorescence, Fluoro-Jade C staining, and neurological score analyses were carried out.

resultsNMNAT2 mRNA and protein levels were increased in the injured-side cortex at 6 hours and peaked 12 hours after TBI. Knocking down NMNAT2 with an injection of small interfering RNA in lateral ventricle significantly exacerbated neuronal degeneration and neurological deficits after TBI, which were accompanied by increased expression of BCL-2-associated X protein (Bax).

conclusionNMNAT2 expression is increased and NMNAT2 exhibits neuroprotective activity in the early stages after TBI, and Bax signaling pathway may be involved in the process. Thus, NMNAT2 is likely to be an important target to prevent secondary damage following TBI.

Indexed as

BCL2 associated XNeurological deficitNeuronal degenerativeNicotinamide nucleotide adenylyltransferase 2Traumatic brain injury

Identifiers

PMID36300321
PMCPMC10323268
OpenAlexW4307429584

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.